IRF5 Antibody
- Known as:
- IRF5 Antibody
- Catalog number:
- 32184
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- IRF5 Antibody
Related genes to: IRF5 Antibody
- Gene:
- IRF5 NIH gene
- Name:
- interferon regulatory factor 5
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-05-31
- Date modifiied:
- 2016-10-05
Related products to: IRF5 Antibody
Related articles to: IRF5 Antibody
- Interferon regulatory factor 5 (IRF5) is genetically linked to ulcerative colitis (UC) susceptibility, yet its role in intestinal inflammation remains poorly understood. Here, we detected IRF5 expression in intestinal tissues from 29 UC patients and 10 healthy controls via immunohistochemistry and immunofluorescence. We constructed DSS-induced acute colitis models in IRF5-knockout (IRF5-/-) and wild-type (IRF5+/+) mice and analyzed the transcriptome of IRF5-knockdown macrophages. IRF5 was highly upregulated in inflamed intestinal tissues of UC patients and DSS-treated mice, primarily in CD68 macrophages. Compared with wild-type mice, IRF5-/- mice exhibited attenuated colitis, with reduced weight loss, lower disease activity index scores and milder colon shortening. Moreover, IRF5 deletion increased anti-inflammatory cytokines (IL-1rn, IL-10, IL-13, IL-17) and decreased pro-inflammatory cytokines (IL-1β, TNF). Transcriptome analysis revealed that IRF5 knockdown suppressed M1 pro-inflammatory genes (Ido1, Il12b) and upregulated the M2 marker MRC2. It also markedly inhibited TLR signaling and actin cytoskeleton regulation. Additionally, IRF5 downregulation reduced Tlr2 expression, indicating a positive feedback loop between IRF5 and TLR signaling. In summary, IRF5 exacerbates intestinal inflammation by promoting M1 macrophage polarization and activating TLR signaling, making it a promising therapeutic target for UC. - Source: PubMed
Publication date: 2026/09/17
Shao LimingChen YiWu LunpoZhong Jing - The interferon regulatory factor (IRF) family exerts dual regulatory roles in vascular inflammation. Pro-inflammatory IRF1/3/5/7 drive endothelial dysfunction, macrophage M1 polarization, vascular smooth muscle cell (VSMC) transdifferentiation, and adaptive immune amplification via nuclear factor-κB (NF-κB), NOD-like receptor pyrin domain-containing 3 (NLRP3), cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING), and Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathways. Conversely, IRF4/8 mediate anti-inflammatory effects by promoting M2 polarization, reverse cholesterol transport, and dendritic cell regulation. In atherosclerosis, IRFs display spatiotemporal specificity: endothelial IRF3 in early stages, macrophage IRF1/5 in mid-stages, and smooth muscle IRF7/IRF8 in late stages, supporting phase-specific precision interventions-early IRF3 blockade, mid-stage modulation of IRF5/IRF4 balance, and late combined inhibition of IRF7/8 to stabilize plaques. IRFs also critically participate in hypertensive remodeling, acute coronary syndrome, heart failure, and aortic aneurysm through conserved innate and adaptive immune axes, highlighting their potential as cross-disease biomarkers and therapeutic targets. Major challenges include network redundancy and functional compensation, necessitating single-cell multi-omics and targeted delivery systems for spatiotemporally precise, individualized modulation. - Source: PubMed
Publication date: 2026/08/26
Bai ChenxiLiu WeixuWang YuboZhu HuixiaFan Xing - Fibrocytes represent a distinct somatic cell type derived from peripheral blood leukocytes, first described as spindle-shaped adherent cells with dual hematopoietic and mesenchymal features. Although fibrocytes were identified in early descriptive studies across several mammalian systems, most of this work predated modern molecular approaches, and the cells remain incompletely defined at the molecular level and have not previously been derived or characterized in cattle. Seeking somatic cells that could be collected aseptically and reproducibly under field conditions for reprogramming to pluripotency, we recognized fibrocytes as a practical and previously unexplored candidate population. Here, we establish a reproducible method for fibrocyte derivation and expansion from adult bovine blood and define their molecular identity using transcriptomic and network analyses. Principal component and differential expression analyses revealed extensive immune, inflammatory, metabolic, and stress-responsive pathways that distinguished fibrocytes from fibroblasts. Upstream regulator analysis identified a fibrocyte-restricted transcriptional network governed by SPI1, IRF5/IRF7, NFKBIZ, PRDM1, CIITA, and MAFB, supporting a monocyte-derived origin and indicating some retention of hematopoietic lineage memory despite acquisition of mesenchymal features. Optimized fibrocyte medium (FbC; dexamethasone, ascorbate, PDGF-BB, EGF, A83-01, CHIR99021) supported stable proliferation and selectively enhanced cytoskeletal and matrix-constructive programs while attenuating inflammatory tone. As proof-of-principle, fibrocytes reprogrammed with polycistronic OCT4-SOX2-KLF4-cMYC and SV40 large T antigen, fibrocytes generated induced pluripotent stem cell (iPSC) colonies exhibiting defining molecular and morphological features of pluripotency. These findings establish fibrocytes as a field-adaptable, stably expandable, and reprogrammable somatic cell type with practical applications in induced pluripotent stem cell generation, genetic preservation, and reproductive biotechnology. - Source: PubMed
Publication date: 2026/09/14
Sylvester HannahKoganti Prasanthi PGurung ShaileshPillai Viju VSelvaraj Vimal - The dysregulated inflammatory response, particularly the interleukin 6 (IL-6)-driven cytokine storm, is a hallmark of severe COVID-19. Mononuclear phagocytes are key cellular populations in the pathogenesis of SARS-CoV-2 infection, but the underlying regulatory mechanisms remain incompletely defined. Based on existing evidence of vitamin D immunomodulatory properties in viral infections, we investigated its role during SARS-CoV-2 infection. We integrated transcriptional profiling of monocytes and myeloid dendritic cells (mDCs) from healthy individuals and COVID-19 patients (moderate/severe, with/without viremia) with an in vitro model of SARS-CoV-2-infected monocyte-derived macrophages (MDMs). Additionally, a functional assay using U937-derived monocytes and macrophages challenged with inactivated SARS-CoV-2 particles was used to assess the immunomodulatory effect of calcitriol (vitamin D) treatment. We found that SARS-CoV-2 infection triggers an NF-κB-dependent inflammatory signature associated with disease severity, both in monocytes from COVID-19 patients and in MDMs infected in vitro. This signature is characterized by hyperproduction of IL-6 and upregulation of its signaling components, including IL6R, JAK1/2, STAT3, and SOCS3. Moreover, we found some evidence of a novel viral-dependent suppression of the Vitamin D Receptor (VDR) pathway, demonstrated by downregulation of both VDR expression and its target genes, including CAMP, LYZ, and IRF5, in monocytes from patients with COVID-19 and in vitro SARS-CoV-2-infected MDMs. This resulted in functional impairment of VDR signaling. Importantly, calcitriol treatment potently suppressed SARS-CoV-2-induced IL-6 production in our model of U937 cell line, suggesting that restoration of VDR signaling could temper this key inflammatory axis. Our findings reveal a dual-hit mechanism in severe COVID-19, in which SARS-CoV-2 infection simultaneously hyperactivates the pro-inflammatory pattern-recognition receptors/NF-κB/IL-6 axis and suppresses the anti-inflammatory VDR pathway in mononuclear phagocytes. The effective inhibition of IL-6 by calcitriol provides a potential role of vitamin D in mitigating pathological inflammation, positioning it as a plausible immunomodulatory strategy for severe COVID-19. - Source: PubMed
Publication date: 2026/09/11
Valdés-López Juan Felipedi Filippo DianaPenagos SharonHernández-Sarmiento Lady JohanaArroyave-Ospina Johanna CRojas MauricioUrcuqui-Inchima SilvioAguilar-Jiménez WbeimarNavas Maria-Cristina - Nucleic acid sensing by endolysosomal Toll-like receptors is critically involved in systemic lupus erythematosus (SLE) and related autoimmune diseases. Downstream of TLR7, TLR8, and TLR9, the SLE-associated SLC15A4-TASL complex selectively mediates IRF5 activation, while being dispensable for NF-κB and MAPK pathways. Here, we show that the SLC15A4-TASL signaling axis is broadly required for disease development and pathogenesis across three complementary genetic SLE models, reflecting different etiologies. Genetic ablation of () and its paralogue () ameliorated or fully prevented autoimmune manifestations resulting from loss of function, respectively. Furthermore, SLC15A4-TASL complex deficiency was sufficient to protect from disease, including splenomegaly, immune activation, and autoantibody formation, driven by the patient-derived gain-of-function mutation, even in the presence of functional NF-κB and MAPK responses. Last, splenocyte transfer into lymphopenic -deficient mice demonstrated that protection extends to DNA-driven autoimmunity, in which TLR7 and TLR9 act redundantly, strongly supporting a B cell-intrinsic role. Notably, SLC15A4-TASL complex deficiency blunted the generation of pathogenic age-associated B cells in all three autoimmune models as well as in aged animals. Collectively, these data demonstrate the central role of the SLC15A4-TASL complex in SLE, supporting its potential as therapeutic target. - Source: PubMed
Publication date: 2026/09/01
Drobek AlesDelacrétaz MaevaVasilakou AlikiMonguió-Tortajada MartaBernaleau LéaDubois MaximeSisirak VanjaRebsamen Manuele